Persistent Elevation Of Blood Pressure Research Articles

Nitric oxide synthase inhibitors cause sustained, but reversible, hypertension and hindquarters vasoconstriction in Brattleboro rats

Homozygous male Brattleboro rats were given a solution of N G-monomethyl-L-arginine (L-NMMA; 1 mg ml −1) to drink for a period of 7 days. There was a persistent elevation of mean arterial blood pressure, accompanied by a significant hindquarters vasoconstriction. Within 9 h of withdrawal of L-NMMA all variables were not different from pre-L-NMMA values. Brattleboro rats (n = 3) which had been drinking N G-nitro-L-arginine methyl ester (L-NAME) solution (0.05 mg ml −1) for 5–6 months showed an increased blood pressure which reversed to normal within 48 h after withdrawing the L-NAME. Thus, inhibition of nitric oxide synthesis leads to long-lasting, but reversible, hypertension.

Increased Familial Cardiovascular Mortality in Obese Schoolchildren: The Muscatine Ponderosity Family Study

Total and cause-specific mortality was investigated in 387 first- and second-degree deceased adult relatives of three groups of children selected from those who participated in three biennial school surveys in Muscatine, Iowa: the lean group (students in the first quintile of relative weight on all three surveys); the random group (a random sample of all eligible students); and the heavy group (students in the fifth quintile of relative weight on all three surveys). A greater proportion of death certificates for heavy group relatives listed a cardiovascular cause of death (60%) compared with lean (48%) and random (43%) group relatives. The relative risk of dying of cardiovascular disease for heavy group vs random group relatives was 1.41 (95% confidence interval 1.01, 1.98). In a subset of heavy group families identified by children with elevated systolic blood pressure, the proportion of death certificates listing a cardiovascular cause was even higher (76%) and the estimate of relative risk vs random group relatives was 2.20 (95% confidence interval 1.43, 3.37). These results indicate that persistent obesity in children, particularly when accompanied by persistent blood pressure elevation, identifies families whose members are at increased risk of dying of cardiovascular disease.

Changes in 24 hour blood pressure and in cardiac and vascular structure in normotensive subjects with parental hypertension.

Subjects with family history of hypertension represent a suitable model to investigate the mechanisms responsible for early cardiovascular structural and functional changes occurring in essential hypertension. In our study we have addressed the factors involved in determining the mild elevation in office blood pressure frequently observed in normotensive subjects with hypertensive parents. In 15 normotensive subjects with both parents hypertensive (FH++) and in 15 normotensive subjects with one parent hypertensive (FH(+)-) we found no evidence of a hyperreactivity to stress as compared to the responses of 15 normotensive subjects with no parental hypertension (FH--). On the contrary FH++ subjects were characterized by a significant although mild increase in their blood pressure values recorded either at rest and in ambulatory conditions over the 24 hours, including night sleep. FH++ and FH(+)- subjects also showed a greater left ventricular mass thickness and a greater minimal forearm vascular resistance than FH-- subjects. Thus, the elevation in blood pressure found in the pre-hypertensive stage in subjects with positive family history for hypertension does not reflect a hyperreactivity to the stress associated with physician's visit but indicates an early and persistent blood pressure elevation. This blood pressure elevation is accompanied by early cardiovascular structural changes which may indicate that these subjects are exposed to a higher risk even before developing overt hypertension.

Persistent elevation of blood pressure among children with a family history of hypertension: the Minneapolis Children's Blood Pressure Study.

We examined the blood pressure of children with and without a family history of hypertension in a longitudinal study. Supine blood pressures were first measured in schoolchildren (mean age 8 years) in 1978 and then on nine more occasions until 1986. Blood pressures of parents were measured in the seated position and their medical histories were obtained in home interviews carried out between 1978 and 1979. Children with a family history of hypertension had a higher mean systolic blood pressure (SBP) at the first screening compared to children without such a family history. This difference persisted at each of the succeeding nine school visits. The parents in hypertensive families had a lower income, greater body weight, were less well-educated and were more likely to be black than parents in families without a history of hypertension. Mothers in hypertensive families were more likely to have a history of heart disease and elevated blood pressure during pregnancy than mothers in normotensive families. The correlations between blood pressure of mothers and their children tended to be higher than those between fathers and their children. Elevated blood pressure emerges well before adolescence among children with a family history of hypertension and the family environment appears to play an important role in its development.

Sleep apnea-associated hypertension and reversible left ventricular hypertrophy

Children with sleep apnea syndrome may have persistent marked elevation of systemic blood pressure, 1,2 which is potentially reversible in adolescents 3 and adults 4' s when the underlying apnea is effectively treated. The occurrence and potential reversibility of marked left ventricular hypertrophy associated with this secondary form of hypertension has not, to our knowledge, been previously reported: We report two siblings with significant hemodynamic complications of this syndrome. CASE REPORTS Patient 1. This black male patient was first seen at age 2 years because of severe respiratory distress after a 5-day history of cough and congestion. In the emergency room, he was unresponsive, with perioral cyanosis and poor air exchange. His weight (22.7 kg) was >95th percentile for age, and height was 86 cm (30th percentile for age). His initial blood pressure was 155/78 (>90th percentile for age and sex), but increased to a maximum of 200/130 within 12 hours. This was controlled initially with nitroprusside intravenously, then captopril and chlorothiazide orally. During this hospitalization, he required prolonged ventiiatory support, bronchodilati0n, and therapy for hypertension and heart failure. The chest radiograph showed cardiomegaly, and M-mode echocardiogram showed a large left ventricular diameter (4.2 cm), increased mass (49 g), and elevated right (0.52) and left (0.44) ventricular systolic time interval ratios. Measurements of the left ventricular posterior wall (0.6 cm) and septum (0.6 cm) were slightly increased for age and height. 6 A morning serum cortisol concentration was normal, as were results of thyroid function studies, serum lipid values, and bone age. He was eventually discharged with a diagnosis of severe bronchospasm leading to respiratory failure and congestive heart failure. For blood pressure control, captopril and chlorothiazide were pr escribed, with a 1200-calorie diet and sodium intake restriction. With this regimen, serial blood pressure measurements were normal (106/60 supine) for age and sex. Other medications included metaproterenol and phenobarbital.

Personal control over work pace--circulatory, neuroendocrine and subjective responses in borderline hypertension.

Cardiovascular and neuroendocrine reactivity during arithmetic task performance were studied in 24 patients with borderline hypertension and normotensive controls. Personal control (self-paced versus externally paced performance) resulted in an attenuated blood pressure (BP) response to task performance in normotensives but not in borderline hypertensives. In response to self-paced work, systolic blood blood pressure (SBP) reactivity was significantly greater in borderline hypertensives, but the heart rate (HR) reactivity was similar in borderline hypertensives and normotensives under the different pacing conditions. Task difficulty (pace variation during external pacing) did not differentially affect reactivity in borderline hypertensives and normotensives. Venous plasma noradrenaline and adrenaline were unaffected by task performance. At rest after the task performance plasma noradrenaline was elevated in both normotensives and borderline hypertensives. The latter group also showed a persistent elevation of diastolic blood pressure after task performance, suggesting a prolonged vasoconstrictor response. The present findings indicate that, in terms of circulatory responses, borderline hypertensives may profit less than normotensives from personal control over environmental demands.

Mass screening of blood pressure in school children: results of the Karatsu Study.

The purpose of this study was to determine the prevalence of persistent blood pressure elevation in school children. Mass screening of blood pressure was performed simultaneously with a cardiovascular health check in school children. Forty four hundred and eighty school children were selected as subjects for this study, consisting of 2289 first grade primary school students aged six and seven (group A), and 2191 second grade junior high school students aged thirteen and fourteen (group B). Of the 4480 students, 4031 were examined at the initial blood pressure screening. Three hundred and sixty students whose systolic and/or diastolic pressures were above the 95th percentile were recalled for a second examination. Three hundred and thirty one students were studied at the 2nd examination, and 69 students were listed for a third survey. 1.7% of the original subjects were examined at the final survey. At the first screening, mean blood pressures were 101.5 +/- 8.5/61.2 +/- 6.6 mmHg (mean +/- SD) for males and 100.3 +/- 8.3/60.9 +/- 6.5 for females in group A. In group B, blood pressures were 120.2 +/- 11.3/66.6 +/- 7.4 mmHg for males and 117.4 +/- 11.2/66.9 +/- 7.8 mmHg for females. This screening system, if incorporated into the school health program, is an effective and efficient method of screening for persistent blood pressure elevation in school children in Japan.

Analysis of mass hypertension screening

Mass screening for high blood pressure is one means of identifying a significant portion of the hypertensive population. In one weekend 30,329 adults were screened and 35% (8,875 of 25,284 with complete data) were referred for high blood pressure. Although this was a self-selected population, these results are similar to other studies of Southern populations. Racial differences were notable in that 36.7% of blacks were referred as compared to 30.5% for whites, with blacks having a higher rate for both systolic and diastolic hypertension. Males had a higher percentage of high blood pressure than females at every level of diastolic hypertension. Of those 49.8% having a prior history of hypertension, 70% were already on therapy, but only 36% of this group had blood pressures within the normal adult range, leaving 8,875 individuals (87%) who were either unaware, untreated or had persistent elevation of blood pressure in spite of therapy. A follow-up program is in progress, and at least 30% have gone to their own physician or clinic for secondary screening. Mass screening is a feasible and relatively inexpensive method for detection of hypertensives, but should only be one aspect of a large-scale coordinated community hypertension control program. In addition, public interest generated from mass screenings is a positive factor in increasing the health awareness of cardiovascular disease and its associated mortality.

THE EFFECT OF ANGIOTENSIN INFUSION, SODIUM LOADING AND SODIUM RESTRICTION ON THE RENAL AND CARDIAC ADRENERGIC NERVES

The renal and cardiac adrenergic nerve patterns in rats infused with large and small amounts of angiotensin and in rats given NaCl plus DOCA, NaCl alone, and salt-free diets were examined by the histochemical fluorescence method. Infusion of small amounts of angiotensin led to a persistent blood pressure elevation whereas infusion of large amounts of angiotensin resulted in a transient rise in blood pressure, probably due to the development of tachyphylaxis. Nerve patterns were found to be normal in angiotensin-infused rats and in rats given NaCl. In rats given NaCl plus DOCA and in rats subjected to salt restriction, a partial or complete disappearance of the transmitter of the adrenergic nerve terminals were recorded. The findings suggest that angiotensin in itself is incapable of inducing visible alterations in the transmitter content of the terminals. The findings agree with the view that angiotensin potentiates a norepinephrine depletion of the terminals during sympathetic activity, since it can be assumed that increased plasma angiotensin levels as well as various degrees of increased sympathetic tonus were present in the rats subjected to salt restriction. The similar effect on the nerve terminals produced by the combined NaCl and DOCA administration is consistent with earlier reports of an increased turnover of norepinephrine in animals thus treated.

Iatrogenic Renal Hypertension:

Two young men with familial extra-adrenal pheochromocytoma (paraganglioma) had almost identical tumors removed with similar postoperative courses, complicated by development of other causes of hypertension. Renal ischemia and persistent blood pressure elevation occurred in both patients but were caused by different anatomic defects. One developed retroperitoneal fibrosis that gradually obstructed renal blood flow to the right kidney; the second patient had a small aberrant artery to the inferior pole of the kidney ligated with prompt development of hypertension. Nephrectomy was necessary in the first patient; segmental resection of the ischemic portion of the kidney was sufficient to interrupt the renin-angiotensin system and allow the blood pressure to return to normal in the second patient.

Iatrogenic renal hypertension: two unusual complications of surgery for familial pheochromocytoma.

Two young men with familial extra-adrenal pheochromocytoma (paraganglioma) had almost identical tumors removed with similar postoperative courses, complicated by development of other causes of hypertension. Renal ischemia and persistent blood pressure elevation occurred in both patients but were caused by different anatomic defects. One developed retroperitoneal fibrosis that gradually obstructed renal blood flow to the right kidney; the second patient had a small aberrant artery to the inferior pole of the kidney ligated with prompt development of hypertension. Nephrectomy was necessary in the first patient; segmental resection of the ischemic portion of the kidney was sufficient to interrupt the renin-angiotensin system and allow the blood pressure to return to normal in the second patient.

Studies on renin. I. Purification of dog renin and micromethod for the determination of renin in dog serum and tissues.

Dog renin was produced with a yield of 1.1 Goldblatt units (GU)/g renal tissue and with a specific activity of 1.3 GU/mg protein, i.e., a specific activity 10-16 times higher than that of previous preparations. This renin, free of angiotensinase and of anaphylactoid substances, was used to study the effects of prolonged infusion of renin in normal conscious dogs and as a standard for the bioassay of renin. A simplified method was designed for the indirect assay of canine renin. After prolonged incubation, the angiotensin produced was determined by bioassay in the rat, and the final estimate was expressed as the concentration of renin, in terms of GU, with an accuracy of ± 12.8%. The lower sensitivity of the assay is 1.0 x 10 -5 GU/ml; this limit permits an estimate of the endogenous renin in 0.1 ml of normal dog serum or in 0.005 mg of normal canine renal tissue. The sensitivity of this bioassay is, therefore, within the range found in seven radioimmunoassays (0.26 x 10 -5 GU/ml to 6.2 x 10 -5 GU/ml), and compared with the previous direct bioassay of renin in the dog the sensitivity is approximately 100,000-fold greater. By reference to an internationally accepted unit of renin, the Goldblatt unit, it was possible to recalculate and compare directly the results obtained in seven laboratories on the concentration of renin in blood, renal lymph, and various other tissues. This unified method for the evaluation of renin assays has made possible the determination of the rate of release of renin from the kidneys and the minimum rate of infusion of renin capable of producing persistent appreciable elevation of blood pressure.

BIOCHEMICAL DISTURBANCES IN HYPERTENSION

<h3>To the Editor:</h3> —The demonstration of a biochemical disturbance is an aid to the understanding of the basic process in any disease. In the disease state of hypertension, there is no agreement as yet on the existence of any such basic disturbance. There is agreement only on the physical disturbance of elevated intraarterial pressure and the morphological lesions as being fundamental characteristics of the disease process. Three of the present methods of producing chronic elevation of blood pressure in experimental animals are (1) treatment with high sodium chloride intake plus daily injections of desoxycorticosterone; (2) the production of disturbed renal blood flow by such methods as artificial constriction of the renal artery, as first demonstrated by Goldblatt (Studies on Experimental Hypertension: Production of Persistent Elevation of Systemic Blood Pressure by Means of Renal Ischemia,<i>J. Exper. Med.</i><b>59</b>:347, 1934) or by a tie placed around the kidney; and (3)

Use of piperoxan and regitine as routine tests in patients with hypertension.

It is generally recognized that persistent elevation of blood pressure and symptoms of ordinary hypertensive vascular disease or essential hypertension occasionally can be caused by secretion of epinephrine from a pheochromocytoma or a paraganglioma. There can exist associated hypertensive retinitis and cardiac or renal abnormality. This type of hypertension often is not recognized as different from the usual variety of unknown etiology. Discovery of the tumor is imperative since removal will effect cure. Therefore, each patient with hypertension should be tested for circulating epinephrine. Goldenberg, Snyder, and Aranow 1 introduced the use of the adrenolytic drug 2-(l-piperidylmethyl)-l, 4-benzodioxan (piperoxan, 933F, or benodaine®), 2 which usually causes a characteristic reduction of blood pressure in patbnts with pheochromocytoma. Grimson and associates 3 used the adrenolytic and sympatholytic drug 2-(N- p -tolyl-N-[ m -hydroxyphenyl]-aminomethyl)-imidazoline hydrochloride (C-7337, or regitine®) 4 before and during operation for pheochromocytoma. This study was undertaken to compare effects of

A CASE OF CHRONIC NEPHRITIS IN CHILDHOOD WITH LATER DEVELOPMENT OF SEVERE HYPERTENSION; RENAL BIOPSY

Case Reports1 May 1949A CASE OF CHRONIC NEPHRITIS IN CHILDHOOD WITH LATER DEVELOPMENT OF SEVERE HYPERTENSION; RENAL BIOPSYEARL I. MULMED, M.D., ARCHIE H. BAGGENSTOSS, M.D., HOWARD B. BURCHELL, M.D.EARL I. MULMED, M.D.Search for more papers by this author, ARCHIE H. BAGGENSTOSS, M.D.Search for more papers by this author, HOWARD B. BURCHELL, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-30-5-1033 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptWhen physical examination reveals markedly increased arterial pressure, determination of the rôle of the kidneys in the causation of this symptom often presents a difficult problem.The question may arise as to whether hypertension of the essential type could occur independently in a case in which evidence of past or latent chronic glomerulonephritis is found. Recently we had the opportunity of studying the histologic appearance of the kidneys and of the arterioles of the skeletal muscles in a case in which the clinical picture was that of severe essential hypertension and in which an established history of chronic glomerulonephritis in...Bibliography1. WAGENERKEITH HPNM: Diffuse arteriolar disease with hypertension and the associated retinal lesions, Medicine, 1939, xviii, 317-430. CrossrefGoogle Scholar2. JOHNSON G: I. On certain points in the anatomy and pathology of Bright's disease of the kidney. II. On the influence of the minute blood-vessels upon the circulation, Trans. Med.-Chir. Soc. London, 1868, li, 57-76. CrossrefGoogle Scholar3. GULLSUTTON WWHG: On the pathology of the morbid state commonly called chronic Bright's disease with contracted kidney ("arterio-capillary fibrosis"), Trans. Med.-Chir. Soc. London, 1872, lv, 273-329. CrossrefGoogle Scholar4. GOLDBLATTLYNCHHANZALSUMMERVILLE HJRFWW: Studies on experimental hypertension. I. The production of persistent elevation of systolic blood pressure by means of renal ischemia, Jr. Exper. Med., 1934, lix, 347-379. CrossrefGoogle Scholar5. PAGE IH: The production of persistent arterial hypertension by cellophane perinephritis, Jr. Am. Med. Assoc., 1939, cxiii, 2046-2048. Google Scholar6. MORITZOLDT ARMR: Arteriolar sclerosis in hypertensive and nonhypertensive individuals, Am. Jr. Path., 1937, xiii, 679-728. Google Scholar7. CASTLEMANSMITHWICK BRH: The relation of vascular disease to the hypertensive state based on a study of renal biopsies from one hundred hypertensive patients, Jr. Am. Med. Assoc., 1943, cxxi, 1256-1261. CrossrefGoogle Scholar8. KERNOHANANDERSONKEITH JWEWNM: The arterioles in cases of hypertension, Arch. Int. Med., 1929, xliv, 395-423. CrossrefGoogle Scholar9. BELL ET: Renal diseases, 1946, Lea & Febiger, Philadelphia, 434 pp. Google Scholar10. DAWSON : Discussion on hyperpiesia, Brit. Med. Jr., 1925, ii, 1161-1163. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication March 24, 1947. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byHerz- und Kreislaufstörungen bei InfektionskrankheitenHerz- und Kreislaufstörungen bei Infektionskrankheiten 1 May 1949Volume 30, Issue 5Page: 1033-1042KeywordsArteriolesBiopsyBlood pressureGlomerulonephritisHypertensionKidneysNephritisSkeletal muscles ePublished: 1 December 2008 Issue Published: 1 May 1949 PDF downloadLoading ...

HYPERTENSION AND THE KIDNEY

Case Reports1 October 1946HYPERTENSION AND THE KIDNEYCARL A. WATTENBERG, M.D.CARL A. WATTENBERG, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-25-4-734 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptUnilateral non-nephritic kidney disease can be the cause of hypertension, and this hypertension often can be relieved by nephrectomy. This fact has been shown definitely. Many case reports have been published since the work by Goldblatt1 and his associates, which should remove any doubt that hypertension may result from certain types of pathological unilateral renal changes. It is true that some of these cases were reported too soon following the nephrectomy, but the urologist still sees nephrectomy as a definite cure for hypertension in certain cases.Certainly there always should be a careful urological examination of all cases of hypertension...Bibliography1. GOLDBLATTLYNCHHANZALSUMMERVILLE HJRFWW: Studies on experimental hypertension. 1. The production of persistent elevation of systolic blood pressure by means of renal ischemia, Jr. Exper. Med., 1934, lix, 347-380. CrossrefGoogle Scholar2. FLOCKS RH: Clinical studies on the relationship between renal disease, renal function and arterial blood pressure, Jr. Urol., 1942, xlvii, 602-613. CrossrefGoogle Scholar3. BRAASCHWALTERSHAMMER WFWHJ: Hypertension and the surgical kidney, Jr. Am. Med. Assoc., 1940, cxv, 1837. CrossrefGoogle Scholar4. BARKERWALTERS NWW: Hypertension and chronic atrophic pyelonephritis, Jr. Am. Med. Assoc., 1940, cxv, 912. CrossrefGoogle Scholar5. BRAASCH WF: Renal disease as a factor in hypertension, Am. Jr. Surg., 1942, lvi, 209-215. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: St. Louis, Missouri*Received for publication July 2, 1945.From the Department of Surgery, Urological Division, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPERIRENAL LYMPHANGIOMA CAUSING HYPERTENSION*JOHN E. PULASKI, M.D. 1 October 1946Volume 25, Issue 4Page: 734-741KeywordsAlbuminsBlood pressureHospital medicineHypertensionKidneysNephrectomyRenal diseasesSurgeryUrine ePublished: 1 December 2008 Issue Published: 1 October 1946 PDF downloadLoading ...

HYPERTENSION CAUSED BY RENAL INFARCTION

Case Reports1 September 1945HYPERTENSION CAUSED BY RENAL INFARCTIONS. BEN-ASHER, M.D.S. BEN-ASHER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-23-3-431 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptOf the numerous experimental investigations as to the pathogenesis of essential hypertension, the work of Goldblatt1is beyond doubt the most outstanding. In a classical experiment he produced hypertension in the dog by constriction of one or both renal arteries with a silver clamp, with a resultant decrease in the blood flow through the kidney. These experiments have been repeated by other investigators with the same result. It is believed that the diminution in renal flow produces hypertension by the secretion of a pressor substance into the blood by the ischemic kidney. Since then a number of reports have appeared...Bibliography1. GOLDBLATTLYNCHHANZALSUMMERVILLE HJRFWW: Studies on experimental hypertension. I. The production of persistent elevation of systolic blood pressure by means of renal ischemia, Jr. Exper. Med., 1934, lix, 347-379. CrossrefGoogle Scholar2. BUTLER AM: Chronic pyelonephritis and arterial hypertension, Jr. Clin. Invest., 1937, xvi, 889-897. CrossrefGoogle Scholar3. BARKERWALTERS NWW: Hypertension and chronic pyelonephritis: results of nephrectomy, Jr. Am. Med. Assoc., 1940, cxv, 912-916. CrossrefGoogle Scholar4. RICHARDS GG: Unilateral renal tuberculosis associated with hypertension, Ann. Int. Med., 1941, xv, 324-328. Google Scholar5. BLATTPAGE EIH: Hypertension and constriction of renal arteries in man; report of case, Ann. Int. Med., 1939, xii, 1690-1699. Google Scholar6. HOWARDFORBESLIPSCOMB TLRPWR: Aneurysm of left renal artery in a child five years old with persistent hypertension, Jr. Urol., 1940, xliv, 808-815. CrossrefGoogle Scholar7. KOONSRUCH KMMK: Hypertension in a seven year girl with Wilms' tumor relieved by nephrectomy, Jr. Am. Med. Assoc., 1940, cxv, 1097-1098. CrossrefGoogle Scholar8. HOFFMAN BJ: Renal ischemia produced by aneurysm of abdominal aorta, Jr. Am. Med. Assoc., 1942, cxx, 1028-1030. CrossrefGoogle Scholar9. PRINZMETALHIATTTRAGERMAN MNLJ: Hypertension in a patient with bilateral renal infarction, Jr. Am. Med. Assoc., 1942, cxviii, 44-46. CrossrefGoogle Scholar10. FISHBERG AM: Hypertension due to renal embolism, Jr. Am. Med. Assoc., 1942, cxix, 551-553. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Jersey City, N. J.*Received for publication July 20, 1944.From the Medical Department of the Fairmount Hospital, Jersey City, N. J. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBlood pressure and renal outcomes in patients with kidney infarction and hypertensionSegmental Renal Artery Infarction: A Case Report With Computerized Tomography Scan and Angiographic CorrelationNatural History of Hypertension in Renal Parenchymal DiseaseRenal Artery Thrombosis: A Cause of Reversible Acute Renal FailurePercutaneous arterial embolization in the kidneys of dogs: a comparative study of eight different materialsHypertension resulting from segmental renal artery infarction A reviewRenal Artery Changes in HypertensionVarious Organic DiseasesMitral Stenosis. Hypertension following Renal EmbolismAkuter ArterienverschlußAcute Renal InfarctionHypertonieHypertonieOcclusion of a Renal Artery as a Cause of HypertensionARTERIAL INFARCTION OF THE KIDNEY*J. GEORGE TEPLICK, M.D., M. WILLIAM YARROW, M.D.Case 38381A CASE OF MALIGNANT HYPERTENSION SECONDARY TO RENAL ISCHEMIA*WILLIAM H. BLAHD, M.D., RAYMOND MARCUS, M.D., DAVID M. WASSERMAN, M.D.Thrombosis of the inferior vena cava and renal veins with hemorrhagic renal infarction in infancyHYPERTENSION FOLLOWING RENAL INFARCTIONRenal Infarction: A Clinical and Possible Surgical EntityThrombosis of the Left Renal Artery with Hyper-Tension: Case Report 1 September 1945Volume 23, Issue 3Page: 431-436KeywordsBlood flowHypertensionInfarctionKidneysPathogenesisRenal arteriesRenal circulation ePublished: 1 December 2008 Issue Published: 1 September 1945 PDF downloadLoading ...

MALIGNANT HYPERTENSION; CURE FOLLOWING NEPHRECTOMY

During the last decade, 1934 to 1944, much clinical interest and experimental effort have been centered on unilateral atrophic pyelonephritis and renal ischemia as causative factors in the production of hypertension. Shortly after the report of the experimental observations of Goldblatt and his associates 1 in 1934 on the production of persistent elevation of systolic blood pressure by means of renal ischemia, there appeared in the literature numerous accounts of the results of nephrectomy in cases of unilateral renal disease and hypertension. Immediate reduction in blood pressure occurred in a considerable number of cases. However, Barker and Walters 2 in 1940 pointed out that although the immediate results in a number of cases were good, the ultimate result of nephrectomy in some cases was not satisfactory with regard to permanent lowering of the blood pressure. In 1941 we 3 reported the case of a girl, 7 years of age, who

CLINICAL PICTURES ASSOCIATED WITH INCREASED BLOOD PRESSURE: A STUDY OF 100 PATIENTS

Article1 October 1939CLINICAL PICTURES ASSOCIATED WITH INCREASED BLOOD PRESSURE: A STUDY OF 100 PATIENTSJ. R. WILLIAMS JR., T. R. HARRISONJ. R. WILLIAMS JR.Search for more papers by this author, T. R. HARRISONSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-13-4-650 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONUntil comparatively recently hypertension has been divided into the "renal" type (including glomerular nephritis and a few rarer disorders of the kidneys) and the "essential" type, the latter term being employed to indicate a rise in blood pressure not due to renal disease. Many clinicians have tended to accept essential hypertension as an entity due to a single but unknown cause. This concept is no longer tenable for two reasons. In the first place the demonstration by Goldblatt and his coworkers1that animals with experimental renal hypertension may present a clinical picture similar in all respects to that of...Bibliography1. GOLDBLATTLYNCHHANZALSUMMERVILLE HJRFWW: Studies on experimental hypertension; production of persistent elevation of systolic blood pressure by means of renal ischemia, Jr. Exper. Med., 1934, lix, 347. CrossrefGoogle Scholar2. FISHBERG AM: Hypertension and nephritis, 1931, Lea & Febiger, Philadelphia, p. 668. Google Scholar3. AYMAN D: Personality type of patients with arteriolar essential hypertension, Am. Jr. Med. Sci., 1933, clxxxvi, 213. Google Scholar4. LEVINEERNSTENE SAAC: Observations on arterial blood pressure during attacks of angina pectoris, Am. Heart Jr., 1933, viii, 323. CrossrefGoogle Scholar5. ALAMSMIRK MFH: Observations in man upon blood pressure raising reflex arising from voluntary muscles, Jr. Physiol., 1937, lxxxix, 372. CrossrefGoogle Scholar6. CUSHING HW: Papers relating to the pituitary body, hypothalamus and parasympathetic nervous system, 1932, Thomas & Co., Springfield. Google Scholar7. PETERS JP: Nature of toxemias of pregnancy, Jr. Am. Med. Assoc., 1938, cx, 329. CrossrefGoogle Scholar8. LONGCOPE WT: Chronic bilateral pyelonephritis: its origin and its association with hypertension, ANN. INT. MED., 1937, xi, 149. LinkGoogle Scholar9. RYTAND DA: Pathogenesis of arterial hypertension in coarctation of the aorta, Proc. Soc. Exper. Biol. and Med., 1938, x, 11. Google Scholar10. SCHROEDERSTEELE HAJM: Abnormalities of the urinary tract in "essential hypertension," Proc. Soc. Exper. Biol. and Med., 1938, xxxix, 107. CrossrefGoogle Scholar11. HARRISON TR: Failure of the circulation, 2nd Ed., 1939, The Williams and Wilkins Co., Baltimore, pp. 396. Google Scholar12. PRINZMETALOPPENHEIMER MET: Rôle of arteries in peripheral resistance to hypertension, Proc. Soc. Exper. Biol. and Med., 1937, xxxvi, 675. CrossrefGoogle Scholar13. BRAUN L: Experimentelle Untersuchungen über Blutdruck und Niere, Wien. klin. Wchnschr., 1933, xlvi, 225 and 1471; Also ibid., 1934, xlvii, 65 and 131. Google Scholar14. GOLDBLATT H: Studies on experimental hypertension; pathogenesis of experimental hypertension due to renal ischemia, ANN. INT. MED., 1937, xi, 69. LinkGoogle Scholar15. BLALOCKLEVY ASE: Studies on etiology of renal hypertension, Ann. Surg., 1937 cvi, 826. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Nashville, Tennessee*Read at the New Orleans meeting of the American College of Physicians March 28, 1939.From the Department of Medicine, Vanderbilt University, Nashville, Tennessee.This work was aided by grants from the Josiah Macy Jr. Foundation, the Rockefeller Foundation, and from Mr. Joe Werthan, Nashville, Tennessee. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byHypertensive Vascular Disease: Its Clinical Course, Differential Diagnosis, Pathogenesis and TreatmentUrologic disease as a cause of hypertensionUrologic hypertension as an entityUnilateral Renal Disease and Renal Vascular Changes in Relation to Hypertension in ManEssential Hypertension, its Nature and Etiology.Hypertension in diphtheria 1 October 1939Volume 13, Issue 4Page: 650-670KeywordsBlood pressureHypertensionKidneysNephritisRenal diseases Issue Published: 1 October 1939 PDF downloadLoading ...

Hypertension from Obstruction of the Aorta

Goldblatt and others have found in chronic experiments that by stenosing the renal arteries and thereby decreasing the blood supply to the kidneys a persistent elevation in blood pressure can be obtained. This phenomenon Goldblatt explains by the hypothesis of a “pressor substance” which he believes is formed as a result of the ischemia of the kidneys. He found also that stenosis of the aorta above the origin of both renal arteries resulted in a persistent elevation of blood pressure while stenosis below the origin of these vessels did not cause hypertension. Rytand, using heart weight increase in rats as evidence of hypertension, obtained similar results. Stenosis of the aorta below the right but above the left renal artery, he found, also produced hypertension; however, if the distal (left) kidney be removed hypertension does not result. Goldblatt's conclusion was that hypertension from experimental aortic stenosis is of the same nature as that due to stenosis of the renal arteries directly, that is, that the stenosis of the aorta caused an elevation of blood pressure by producing renal ischemia. This idea was further expanded by Rytand to the supposition that renal ischemia with its resulting “pressor substance” is the important factor in the elevation of blood pressure so regularly found in the upper extremities in coarctation of the aorta. Inasmuch as these results were obtained in chronic experiments it was felt that it would be interesting to investigate the aortic phenomenon with acute stenosis at similar levels. Using dogs, intraperitoneal nembutal (pentabarbital) as anesthetic and carotid cannula recordings with the kymograph, the following experiments were performed: 1. A screw clamp was placed about the aorta just above the origin of the celiac axis, 2 or 3 cm above the origin of the right (upper) renal artery.